2011 Blackwell Publishing Ltd 49 Companion Animal Vol 16 November 2011

LIFE C,CLE A!D #%E)ALE!CE

E. cuniculi spores are passed in the urine by an
infected host. The spores can survive in the
environment for at least four weeks at room
temperature. Following oral infection, normally
from contaminated food, the spores invade
reticuloendothelial cells in the intestinal mucosa which
then distribute the parasite systemically. Infected cells
rupture, releasing spores to invade new cells. This
provokes an inflammatory response, with subsequent
formation of granulomatous lesions, predominantly
in the kidney and central nervous system. The close
association between young rabbits and their dams
allows easy infection in the first few days of life and,
as a result, prevalence in domestic rabbits is high.
Seroprevalence in the UK has been shown to be
approximately 50% and this makes establishing
whether infection is responsible for clinical signs in
any given patient very difficult to achieve.
Infection in wild rabbits is rare, although they can
easily be infected experimentally. Increased hygiene
and a lower population density in wild rabbit
populations significantly reduce post-natal infection.
Wild rabbits do not act as a significant reservoir of
infection for domestic rabbits.
Although E. cuniculi can infect a range of different
host species, systemic disease is rare in species other
than rabbits and guinea pigs. A zoonotic potential
exists, and although cases are rare, there is the
potential for it to infect humans with acquired
immune deficiency syndrome, causing diarrhoea,
wasting syndromes and pneumonia. At-risk owners
of rabbits should maintain strict hygiene around
rabbits and consider having pets tested for exposure
to E. cuniculi.
CLI!ICAL &IG!&
There are no pathognomonic clinical signs
associated with E. cuniculi infection and many
cases are subclinical. In clinically affected rabbits
disease may be acute or chronic, with three
syndromes commonly observed either individually
or in combination.
Acute CNS or renal syndromes may present as
sudden death and E. cuniculi should be considered
when investigating these cases in rabbits. Stress is a
recognised initiating cause of acute disease in
previously subclinical carriers. Guinea pigs housed
with domestic rabbits are at increased risked of
nephritis but are resistant to cerebral granulomas and
as a result clinical signs are renal rather than
neurological in nature.
!1A>;8;35/-8 ?53:?
Granulomatous lesions in the central nervous system
can lead to neurological signs. The most common of
these are vestibular, e.g. a head tilt (Fig. 1),
hemiparesis and ataxia. In severe cases, patients will
be unable to right themselves and will frequently
spin or fall. Limb paralysis, seizures and urinary
incontinence can occur as well as vague generalised
CNS signs such as swaying, head nodding and
perceived deafness.
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Infection with E. cuniculi leads to granulomatous
interstitial nephritis. This may be subclinical or lead
to renal dysfunction and muscle wastage.
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Cataracts and lens rupture leading to anterior
chamber uveitis can occur, and are usually unilateral.
Vertical transmission can lead to invasion of the lens
while the lens capsule is thin or absent. Affected
Ian Wright BVMS BSc MSc MRCVS
WITHY GROVE VETERINARY CLINIC, 39 STATION ROAD, BAMBER BRIDGE, PRESTON, LANCASHIRE. PR5 6QR
ABSTRACT: E%ce'ha#*&0&&% c+%c+# ) a% %*(ace##+#a( '(&*&0&a% 'a(a)*e &f *he Microsporidia ge%+). A#*h&+gh * ca%
%fec* a %+$be( &f )'ece) &f a%$a#, %c#+d%g $$+%e-c&$'(&$)ed 'e&'#e, * ) '($a(#/ a 'a*h&ge% &f (abb*).
Re#a*,e#/ #**#e -a) "%&-% ab&+* *he 'a(a)*e f&( $a%/ /ea() b+* %c(ea)%g %+$be() &f )*+de) % *he 'a)* decade ha,e
(e,ea#ed $+ch ab&+* *) '(e,a#e%ce a%d *(ea*$e%* a%d %c(ea)%g#/ )h&-% * *& be a c&$$&% %fec*&% &f d&$e)*c
(a*he( *ha% -#d (abb*). DOI: 10.1111/!.2044-3862.2011.00125..
Fig. 1: Rabbit exhibiting head tilt associated
with E. cuniculi infection.
Encephalitozoon cuniculi:
Infecting the rabbit next door
2011 Blackwell Publishing Ltd 50 Companion Animal Vol 16 November 2011
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&A<<;>@5B1 @>1-@91:@
Although elimination of the parasite is sometimes
sufficient to lead to resolution of clinical signs,
supportive treatment may be required. Anti-
inflammatory doses of 01D-91@4-?;:1 by
subcutaneous injection can be useful in improving
or resolving neurological problems, particularly
acute vestibular signs. Treatment with topical and
systemic steroid is essential in treating uveitis, as this
will not resolve with elimination of the parasite.
&E?@195/ -:@5.5;@5/ @>1-@91:@ is required if
secondary pasteurellosis is suspected. I:@>-B1:;A?
28A50? are useful in acute renal cases but clinical
chronic cases carry a poorer prognosis.
C;:@>;8
Control in the laboratory setting is crucial as even
low levels of disease caused by the parasite can
interfere with experimental results. It is common
for laboratory rabbits to be tested routinely for
E. cuniculi antibodies, and positive animals culled.
In the domestic setting, treatment with fenbendazole
at 20 mg/kg PO q 24h for nine consecutive days
four times a year has been shown to be effective in
reducing levels of infection and shedding. Methods
to reduce urine contamination of food, such as
using water bottles, lifting food off the ground and
not using tiered systems of housing, also reduce levels
of infection.
rabbits are usually young when clinical signs occur.
Opportunistic pasteurellosis in rabbits with E.
cuniculi infection can lead to intraocular abscessation
and acute uveitis.
DIAG!"&I&
Diagnosis of E. cuniculi as a cause of on-going disease
is problematic, as so many rabbits are carriers of
infection and there are no pathognomonic signs.
Although it should theoretically be possible to detect
spores in urine as a diagnostic method, difficulty in
collecting rabbit urine in a domestic setting, the
intermittent shedding of spores and the large
amount of sediment that naturally occurs in rabbit
urine makes it impractical in reality.
Serology and post-mortem examination are both
useful diagnostic tools when investigating possible
infection in diseased animals.
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Enzyme-linked immunosorbent assays (ELISAs), to
detect antibodies to E. cuniculi, are available. A serum
antibody response develops by three weeks post
infection and antibody levels can remain high for
many months. Thus demonstrating seropositivity
only indicates previous exposure and does not
confirm current infection.
#;?@-9;>@19 1D-95:-@5;:
Gross post-mortem examination will not allow a
definitive diagnosis of clinical E. cuniculi infection to
be made. Macroscopic lesions are not visible in the
brain. Grossly, the kidneys of infected individuals will
have focal depressed areas giving them a pitted
appearance. Although this is characteristic of
exposure to infection it does not confirm current
infection or that E. cuniculi is the cause of current
disease. Histological examination will demonstrate a
granulomatous interstitial nephritis and in acute
infection ovoid spores may be seen in cells or free in
the collecting tubules. This confirms active infection
but identification of the organism in histological
sections is intermittent in acute disease and absent in
chronic cases as the disease progresses and interstitial
fibrosis occurs. Histological examination of the brain
may reveal granulomatous lesions and, in
combination with CNS signs, is strongly indicative
of clinical encephalitozoonosis. In cases of ocular
disease, E. cuniculi organisms may be observed in the
liquefied lens cortex.
'%EA'E!' A!D C"!'%"L
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Treatment of encephalitozoonosis consists of
elimination of the parasite and supportive treatment.
E8595:-@5;: ;2 @41 <->-?5@1
Fenbendazole, at a dose of 20 mg/kg PO q 24h for
28 days, is the treatment of choice as, unlike
albendazole, it is not teratogenic.
CONTI NUI NG PROFESSI ONAL
DEVELOPMENT SPONSORED BY
BAYER ANI MAL HEALTH
1. E. /A:5/A85 ?<;>1? ->1 ?410:
a. in faeces
b. in urine
c. in seminal fluid
d. in all of the above
2. *45/4 ;2 @41 2;88;C5:3 ;>3-:? 5? - /;99;: ?5@1
2;> 3>-:A8;9-@;A? 81?5;: 2;>9-@5;: -??;/5-@10
C5@4 E. /A:5/A85 5:21/@5;::
a. liver
b. spleen
c. kidney
d. lungs
3. E. /A:5/A85 5? ?1:?5@5B1 @; C45/4 ;2 @41 2;88;C5:3
/419;@41>-<1A@5/ -31:@?:
a. fenbendazole
b. metronidazole
c. ivermectin
d. amoxycillin
e. none of the above
These multiple choice questions are based on the above
text. Answers appear on page 51 of the print version, and
as supporting information in the online version of this article.